It has long been known that a stimulus may be delivered about 300 ms following a primary pacing pulse or about 300 ms following a spontaneous depolarization. These stimuli have the effect of electrically depolarizing the heart but typically they do not induce a separate mechanical myocardial contraction. Instead, they extend or enhance the strength and/or duration of the contraction already induced by a primary pacing pulse. This phenomena is known as pulseless electrical activity (PEA).
When a secondary pulse is delivered about 300 ms following a primary pacing pulse, this is referred to as paired pacing. When a spontaneous depolarization triggers a pacing pulse about 300 ms later, this is referred to as coupled pacing. Coupled pacing has the ability to prolong the refractory period and affects a slowing of the heart by increasing the interval between spontaneous depolarizations. Performing paired pacing also prolongs the refractory period and allows pacing the heart at a rate slower than the intrinsic rate, because the prolonged refractory period delays the spontaneous depolarization.
Many uses for paired/coupled pacing techniques have been proposed. Siddons and Sowton (Cardiac Pacemakers. 1967:201-216) have proposed that paired/coupled pacing may be used to provide continuous extra-systolic augmentation and indeed cardiac performance has been found to be enhanced by this therapy. The objective is to treat heart failure and to enhance cardiac performance in congestive heart failure (CHF). It proved to be effective in these patients but there was great concern that an extra-stimulus provided in the ventricles at an inappropriate time, i.e., during the relative refractory period, would create excessive arrhythmic risk, particularly fibrillation. Such patients are already susceptible to arrhythmias and may be put at an even greater risk by stimulating near the vulnerable period.
Coupled pacing has also been used for treatment of ventricular and atrial tachyarrhythmias in which a stimulus is coupled to a spontaneous depolarization and set to a fraction of the spontaneous cardiac interval as taught by Zacouto (U.S. Pat. No. 3,857,399) and Pequignot (U.S. Pat. No. 3,939,844). This effectively slows the heart during an arrhythmia.
Paired pacing has been proposed in the atrium to augment ventricular contraction but was not found to be as effective as paired ventricular stimulation. Bornzin et al. (U.S. Pat. No. 6,377,852) has proposed that paired stimulation of the atrium may be used to increase the atrial refractory period and prevent premature atrial contractions (PACs) from the left atrium (LA) from triggering reentrant atrial arrhythmias. This technique may be especially effective during LA pacing since it has been shown that inducing atrial arrhythmias from the right atrium is very difficult. Papageorgiu showed that pacing from distal coronary sinus (CS) caused low atrial depolarization rendering it refractory to premature stimuli delivered from HRA and precluded induction of atrial fibrillation. (Papageorgiu et al. “Coronary sinus pacing prevents induction of atrial fibrillation,” CIRC, 1997; 96:1893-1989.) Bornzin has also suggested that paired pacing in the atrium may be used to slow the overall rate to allow more time for filling the ventricle, which may be useful in enhancing stroke volume in patients with diastolic dysfunction. The following patents and patent applications also discuss paired pacing and related techniques: U.S. Pat. No. 5,213,098 to Bennett et al.; U.S. Patent Application 2003/0074029 of Deno et al.; and U.S. Patent Application 2004/0049235 of Deno et al.
None of the foregoing patents or publications, however, provides effective techniques for safely stimulating the heart just outside of the relative refractory period so as to obtain improved cardiac performance through extra-systolic augmentation, with reduced risk of fibrillation induction. It is to this end that aspects of the invention are particularly directed.